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Heart failure (HF) remains a major growing public health problem in the United States. Despite extensive understanding of the mechanism at the molecular level and innovations in therapy, HF carries high morbidity and mortality rates, with frequent hospital admissions. In the Medicare population, HF is the leading cause for hospitalization, accounting for more than1 million admissions per year. The authors provide a review of the epidemiology and pathophysiology of HF., (Published by Elsevier Inc.)

Heart failure (HF) and atrial fibrillation (AF) are highly prevalent debilitating conditions that often coexist and are frequently encountered in clinical practice. The presence of chronic AF is a marker of worse prognosis in patients with HF, and the onset of new AF in those with chronic HF is associated with increased morbidity and mortality. Advances in the development of novel drugs, nonpharmacologic modalities, and therapeutic strategies, as well the increased understanding of the pathobiology of HF and AF, are key to mitigating the tremendous public health burden that is associated with these conditions., (Published by Elsevier Inc.)

Heart failure (HF) is a major public health problem associated with increased morbidity and mortality. As the US life expectancy increases and the population ages, the overall prevalence of HF will continue to escalate. The increasing use of effective selective therapies such as neurohormonal blockade in the treatment of patients with HF has led to considerable improvement in their prognosis. During the past several decades, some studies have demonstrated the benefits of treatment; based on the evidence available from these studies, various national and international guidelines have specific recommendations for the evidence-based therapy with these drugs in patients with HF., (Published by Elsevier Inc.)

The focus of this article is to review the process of left ventricular remodeling and discuss the results of several published large clinical trials that have demonstrated the benefit of early intervention in heart failure to prevent left ventricular remodeling and progression of cardiac dysfunction. The knowledge gained from this review should help define a strategy for the internist to initiate therapy early in the course of development of heart failure.

Several clinical trials have provided compelling evidence in support of the benefits of lipid-lowering therapy for primary and secondary prevention of atherosclerosis. The results of primary prevention trials have demonstrated that coronary morbidity can be reduced and survival improved with effective lipid-lowering regimens. There has been concern, however, regarding harmful effects (e.g., increased rate of suicide and increased risk of gastrointestinal cancer) of cholesterol-lowering therapies in primary prevention trials. These concerns are not well supported by strong evidence, and there has been lack of a dose-response relationship. It is generally believed that for 1% reduction in serum cholesterol, there is a 2% reduction in the risk of coronary events. The results of numerous secondary prevention trials have clearly demonstrated the benefit of lipid-lowering therapies in reducing the risk of future cardiac events and cardiac mortality in patients with preexistent coronary artery disease. Several studies have shown that treatment regimens effective in reducing LDL cholesterol levels lead to regression of atherosclerotic plaques as well as retard the progression of the disease process. Interestingly, some of these studies have also shown that when measured angiographically, the luminal diameter at the site of stenotic lesions might improve only by an average of 2% to 3%; however, this small degree of improvement is associated with a remarkable reduction by 35% to 25% in the risk of future coronary events. These findings further corroborate the hypothesis about the importance of a lipid-rich cap of the vulnerable plaques and suggest that the reduction in lipid levels is associated with the efflux of lipids from the plaque, thus converting it from a vulnerable to a stable state. The most recent data from the 4S trial have unequivocally demonstrated the benefits of treatment with HMG coenzyme-A reductase inhibitors in reducing the risk of future coronary events and improving the overall survival in patients with established CHD. Although there is still ongoing controversy regarding the precise course of action for primary prevention of CHD, the results of a large number of studies provide overwhelming evidence in support of aggressive lipid-lowering therapy for secondary prevention of CHD. Based on the findings of these studies, it seems prudent that clinicians become actively involved in the evaluation and management of lipid abnormalities and other risk factors in patients with CHD.

CAD continues to be the principal cause of mortality in the United States, and the largest group of patients with CAD are those with stable angina. Among this group of patients, the most common manifestation of CAD is presence of transient episodes of myocardial ischemia. The presence of transient ischemia and not the severity of angina has been found to be associated with poor clinical outcome in patients with stable CAD. As part of a global treatment strategy for patients with stable CAD, changes in lifestyle and modification of coronary risk factors should be emphasized as an integral part of treatment. Conventional antianginal therapy is quite effective in controlling anginal attacks. Currently, several drugs and therapeutic strategies are available for the treatment of patients with angina (see Table 5). Nitrates are highly effective antianginal drugs with complex beneficial actions in patients with CAD, but their usefulness is limited by development of tolerance during long-term use. When clinically indicated, the use of nitrates should be supplemented with another longer-acting antianginal drug, such as a beta-blocker or a calcium channel blocker. Based on the available data, beta-blockers, when tolerated, seem to be the most effective antianginal drugs for most patients with stable CAD. Beta-blockers are also the most effective anti-ischemic drugs that reduce the magnitude of myocardial ischemia detected during routine daily activities. Calcium channel blockers are also effective vasodilators and good antianginal drugs. The clinician should become familiar with the different actions that this heterogeneous group of drugs has on the heart and vessels. This knowledge allows the clinician to choose the appropriate combination of different antianginal drugs for patients on an individualized basis. It is also critical to develop the treatment strategy by carefully taking into account other associated medical conditions that are frequently encountered in patients with CAD.